Person-centered methods represent an important advance in the simultaneous examination of multiple indicators of neuroendocrine functioning and may facilitate a more nuanced understanding of the impact of child maltreatment on hypothalamic–pituitary–adrenal axis dysregulation. The aims of the present study were threefold: (a) identify naturally occurring patterns of diurnal cortisol and dehydroepiandrosterone (DHEA) regulation among a sample of N = 1,258 children with and without histories of maltreatment, (b) investigate which neuroendocrine profiles characterize children with exposure to maltreatment, and (c) examine which profiles are related to adaptive outcomes and symptomatology among children. Cortisol and DHEA were sampled three times per day (9 a.m., 12 p.m., and 4 p.m.) across 5 and 2 days, respectively. Four profiles of cortisol and DHEA regulation were identified. Among females, a pattern marked by high cortisol and low DHEA was associated with more pervasive maltreatment experiences. Furthermore, we found evidence of adaptive interpersonal resilience such that children with maltreatment exposure who evidenced this pattern of high cortisol and low DHEA were viewed as more likeable than maltreated children with other neuroendocrine patterns. Finally, results pointed to higher levels of internalizing symptoms among children who displayed a profile marked by average cortisol and high DHEA.

Childhood maltreatment is a potent interpersonal trauma associated with dysregulation of emotional processes relevant to the development of psychopathology. The current study identified prospective links between patterns of maltreatment exposures and dimensions of emotion regulation in emerging adulthood. Participants included 427 individuals (48% Male; 75.9% Black, 10.8% White, 7.5% Hispanic, 6% Other) assessed at two waves. At Wave 1, children (10–12 years) from families eligible for public assistance with and without involvement with Child Protective Services took part in a research summer camp. Patterns of child maltreatment subtype and chronicity (based on coded CPS record data) were used to predict Wave 2 (age 18–24 years) profiles of emotion regulation based on self-report, and affective processing assessed via the Affective Go/No-Go task. Results identified associations between task-based affective processing and self-reported emotion regulation profiles. Further, chronic, multi-subtype childhood maltreatment exposure predicted difficulties with aggregated emotion dysregulation. Exposure to neglect with and without other maltreatment subtypes predicted lower sensitivity to affective words. Nuanced results distinguish multiple patterns of emotion regulation in a sample of emerging adults with high exposure to trauma and socioeconomic stress and suggest that maltreatment disrupts emotional development, resulting in difficulties identifying emotions and coping with emotional distress.

Exposure to childhood maltreatment (CM) may disrupt typical development of neural systems underlying impulse control and emotion regulation. Yet resilient outcomes are observed in some individuals exposed to CM. Individual differences in adult functioning may result from variation in inhibitory control in the context of emotional distractions, underpinned by cognitive–affective brain circuits. Thirty-eight healthy adults with a history of substantiated CM and 34 nonmaltreated adults from the same longitudinal sample performed a Go/No-Go task in which task-relevant stimuli (letters) were presented at the center of task-irrelevant, negative, or neutral images, while undergoing functional magnetic resonance imaging. The comparison group, but not the maltreated group, made increased inhibitory control errors in the context of negative, but not neutral, distractor images. In addition, the comparison group had greater right inferior frontal gyrus and bilateral frontal pole activation during inhibitory control blocks with negative compared to neutral background images relative to the CM group. Across the full sample, greater adaptive functioning in everyday contexts was associated with superior inhibitory control and greater right frontal pole activation. Results suggest that resilience following early adversity is associated with enhanced attention and behavioral regulation in the context of task-irrelevant negative emotional stimuli in a laboratory setting.

As a founder of the field of applied developmental psychology, Dr Edward Zigler promoted public policy that translated scientific knowledge into real-world programs to improve the outcomes of high-risk children and families. Many researchers, practitioners, and public policy proponents have sought to carry on his legacy through integration of empirical research, evidence-based prevention and intervention, and advocacy to address a range of challenges facing families with young children. To advance the field of child maltreatment, a multidisciplinary team of investigators from the Universities of Rochester and Minnesota partnered with the Eunice Kennedy Shriver National Institute of Child Health and Human Development to create the Translational Research that Adapts New Science FOR Maltreatment Prevention Center (Transform). Building on state-of-the-art research methodologies and clinical practices, Transform leverages theoretically grounded research and evidence-based interventions to optimize outcomes for individuals across the life span who have experienced, or may be at risk for, maltreatment. Inspired by the work of Dr Zigler, Transform is committed to bridging science and real-world practice. Therefore, in addition to creating new science, Transform's Community Engagement Core provides translational science to a broad audience of investigators, child-serving professionals, and parental and governmental stakeholders. This article describes Transform's purpose, theoretical framework, current activities, and future directions.

Few conditions epitomize severe and chronic stress to a greater extent than child maltreatment, which can derail development across multiple domains of functioning and throughout the life course. Furthermore, child maltreatment tends to co-occur with other adversities, such as poverty. Many individuals grow up under the stressful conditions of these adversities and exhibit developmental competence. The current study prospectively charted the developmental progression of economically disadvantaged maltreated and nonmaltreated children from childhood to emerging adulthood, and examined patterns of competence across multiple developmental domains of functioning central to the period of emerging adulthood. The study investigated childhood precursors to these patterns of adaptation and maladaptation, as well as the physiological cost of these patterns of adaptation (i.e., C-reactive protein; CRP). Latent class analysis revealed four distinct classes of functioning: multifaceted competence across domains (Multifaceted Competence); (multifaceted maladaptation across domains (Multi-Problem); (c) and two classes with mixed patterns of competence and maladaptation (Externalizing Problems and Work/School Impairment). Maltreated individuals were less likely than nonmaltreated individuals to demonstrate patterns of multifaceted competence and more likely to demonstrate aggregate maladaptation across domains. Additionally, Black men who demonstrated a pattern of multifaceted psychosocial competence also evidenced higher levels of low-grade inflammation (indexed by CRP), suggesting physiological distress was associated with adaptation in the context of stress among these individuals. Findings demonstrate the heterogenous patterns of functioning and diverse developmental outcomes that follow early adversity.

Teenage childbearing (age 15–19 years) represents a significant public health issue that can generate considerable deleterious, multigenerational consequences for teen-childbearing mothers and their offspring. However, few studies have examined the potential mediating mechanisms that may explain if and how teen childbearing is associated with the development of offspring psychopathology. The current study used a developmental model to test the mediating role of chronic child maltreatment in the relationship between teen childbearing and offspring internalizing symptoms in childhood and emerging adulthood. The study participants were 384 individuals from socioeconomically disadvantaged, ethnically diverse backgrounds, assessed across two longitudinal waves of data (i.e., ages 10–12 and 18–20). The sample included maltreated and nonmaltreated children, all of whom were comparable in terms of family income. Structural equation modeling was conducted to test direct and indirect pathways from teen childbearing to offspring psychopathology. A multigenerational developmental cascade was found such that individuals born to mothers who began their childbearing in adolescence were more likely to experience chronic maltreatment during childhood, which in turn predicted greater internalizing symptoms throughout childhood and emerging adulthood. Using a developmental psychopathology framework, the results are discussed with regard to implications for prevention and early intervention.

Maltreatment during childhood is associated with difficult interpersonal relationships throughout the life course. The aim of the current study was to investigate differential pathways from child maltreatment to emerging adult relationship dysfunction. Specifically, we prospectively tested whether child maltreatment initiates a developmental cascade resulting in coercive negative romantic and friend interactions in emerging adulthood via childhood antisocial tendencies and via childhood relational aggression. Utilizing a longitudinal sample of emerging adult participants (N = 392; mean age = 20 years old) who took part in a summer research camp program as children (mean age = 11 years old), results supported pathways via both childhood antisocial behavior and childhood relational aggression. We found specificity within these pathways such that childhood antisocial behavior was a mediator of child maltreatment effects on emerging adult negative romantic interactions, whereas childhood relational aggression was a mediator of child maltreatment effects on emerging adult negative friend interactions. Taken together, results indicate that children exposed to maltreatment face significant interpersonal challenges in emerging adulthood, within both the friend and the romantic domains, and point to distinct childhood pathways to these negative interactions. Our findings are consistent with Dishion's (2016) theoretical framework for understanding the development of coercion in relationships and highlight the criticality of early intervention with maltreating families.

This study used a structural equation mixture model to examine associations between child maltreatment, polygenic risk, and indices of adaptive functioning. Children aged 6 to 13 years (N = 1,004), half maltreated, half nonmaltreated, were recruited to attend a research day camp. Multi-informant indicators of prosocial behavior, antisocial behavior, withdrawn behavior, and depression were collected and used in a latent class analysis. Four classes emerged, characterizing “well-adjusted,” “externalizing,” “internalizing,” and “socially dominant” groups. Twelve genetic variants, previously reported in the Gene × Environment literature, were modeled as one weighted polygenic risk score. Large main effects between maltreatment and adaptive functioning were observed (Wald = 35.3, df = 3, p < .0001), along with evidence of a small Gene × Environment effect (Wald = 13.5, df = 3, p = .004), adjusting for sex, age, and covariate interaction effects.

The present study tested the role of FKBP5 binding protein 5 (FKBP5) genetic variation in an internalizing pathway from child maltreatment to emerging adult problem drinking among a sample of African American youth (N = 280) followed prospectively from ages 11 to 20. Specifically, whether childhood internalizing symptoms and emerging adult tension reduction alcohol expectancies sequentially mediate the effect of child maltreatment on emerging adult problem drinking and whether FKBP5 moderates these associations were investigated. The results indicate that individuals with at least one copy of the FKBP5 CATT haplotype (minor alleles) are more vulnerable to traversing the hypothesized internalizing pathway of risk than individuals without this genotypic profile. Taken together our findings highlight the importance of FKBP5 genetic variation in the context of early adversity; support the role of two prospective sequential mediators of an internalizing pathway to problematic drinking, namely, childhood internalizing symptoms and emerging adult tension reduction alcohol expectancies; and identify a subgroup of maltreated children most susceptible to progressing along this less common pathway of risk.

Numerous investigations have demonstrated that child–parent psychotherapy (CPP) promotes secure attachment between mothers and offspring. However, the role of postintervention attachment security as it relates to long-term child outcomes has never been evaluated. The present study therefore examined postintervention attachment status as a mediator of the association between CPP for depressed mothers and their offspring and subsequent peer relations among offspring. Depressed mothers and their toddlers were randomized to receive CPP (n = 45) or to a control group (n = 55). A prior investigation with this sample indicated that offspring who received CPP attained significantly higher rates of secure attachment postintervention, whereas insecure attachment continued to predominate for offspring in the control group. The present study examined follow-up data of teachers’ reports on participants’ competence with classroom peers when they were approximately 9 years old. Findings indicated that children who received CPP were more likely to evidence secure attachments at postintervention, which in turn was associated with more positive peer relationships at age 9.

Using a developmental cascades framework, the current study investigated whether treating maternal depression via interpersonal psychotherapy (IPT) may lead to more widespread positive adaptation for offspring and mothers including benefits to toddler attachment and temperament, and maternal parenting self-efficacy. The participants (N = 125 mother–child dyads; mean mother age at baseline = 25.43 years; 54.4% of mothers were African American; mean offspring age at baseline = 13.23 months) were from a randomized controlled trial of IPT for a sample of racially and ethnically diverse, socioeconomically disadvantaged mothers of infants. Mothers were randomized to IPT (n = 97) or an enhanced community standard control group (n = 28). The results of complier average causal effect modeling showed that engagement with IPT led to significant decreases in maternal depressive symptoms at posttreatment. Moreover, reductions in maternal depression posttreatment were associated with less toddler disorganized attachment characteristics, more adaptive maternal perceptions of toddler temperament, and improved maternal parenting efficacy 8 months following the completion of treatment. Our findings contribute to the emerging literature documenting the potential benefits to children of successfully treating maternal depression. Alleviating maternal depression appears to initiate a cascade of positive adaptation among both mothers and offspring, which may alter the well-documented risk trajectory for offspring of depressed mothers.

This paper reports the first large-sample investigation of the maltreatment-related correlates of low-income adolescents’ narratives about their childhood experiences with primary caregivers, as assessed with a modified version of the Adult Attachment Interview (AAI) and based on official reports of abuse and neglect (maltreated n = 214, nonmaltreated n = 140; M age = 16.7 years). Drawing on factor-analytic and taxometric evidence indicating that AAI narratives vary along two state of mind (i.e., dismissing and preoccupied) and two inferred childhood experience (i.e., maternal and paternal) dimensions, here we demonstrate that the experience of maltreatment, particularly when chronic, is associated with increased risk for dismissing and preoccupied states of mind and more negative inferred childhood experiences. Although such maltreatment-related associations were generally not specific to any of the four AAI dimensions, the experience of physical and/or sexual abuse was uniquely associated with preoccupied states of mind and negative inferred paternal experiences even after controlling for the other AAI dimensions. More extensive paternal perpetration of maltreatment also was uniquely related to more negative inferred paternal experiences.

The FK506 binding protein 5 gene (FKBP5) has been associated with susceptibility to pathogenic effects of childhood trauma including dissociative symptoms. This study examines the impact of maltreatment on dissociative tendencies in adolescence as moderated by the FKBP5 gene. Dissociative symptoms and variation within FKBP5 were assessed in a high-risk, low socioeconomic status community sample of 279 maltreated and 171 nonmaltreated adolescents. Following the assignment of haplotypes across four single nucleotide polymorphisms (rs3800373, rs9296158, rs1360780, and rs9470080), individuals with one or more copies of the CATT haplotype (N = 230) were grouped together and compared to individuals with zero copies of this haplotype (N = 185). Analyses of covariance were conducted to test hypotheses regarding the effects of developmental timing and the chronicity of maltreatment and the CATT haplotype. We found a significant interactive effect of timing/chronicity of maltreatment and the CATT haplotype on dissociative symptoms. Among adolescents who had no copies of the CATT haplotype, dissociative symptoms were higher for chronically maltreated adolescents who had an infancy onset compared to those who were not maltreated or whose maltreatment experience was either relatively less chronic or not started in infancy. The groups did not differ significantly among subjects who carry one or more copies of the CATT haplotype.

In the present investigation, differential methylation analyses of the whole genome were conducted among a sample of 548 school-aged low-income children (47.8% female, 67.7% Black, M age = 9.40 years), 54.4% of whom had a history of child maltreatment. In the context of a summer research camp, DNA samples via saliva were obtained. Using GenomeStudio, Methylation Module, and the Illumina Custom Model, differential methylation analyses revealed a pattern of greater methylation at low methylation sites (n = 197 sites) and medium methylation sites (n = 730 sites) and less methylation at high methylation sites (n = 907 sites) among maltreated children. The mean difference in methylation between the maltreated and nonmaltreated children was 6.2%. The relative risk of maltreatment with known disease biomarkers was also investigated using GenoGo MetaCore Software. A large number of network objects previously associated with mental health, cancer, cardiovascular systems, and immune functioning were identified evidencing differential methylation among maltreated and nonmaltreated children. Site-specific analyses were also conducted for aldehyde dehydrogenase 2 (ALDH2), ankyrin repeat and kinase domain containing 1 (ANKK1), and nuclear receptor subfamily 3, group C, member 1 (NR3C1) genes, and the results highlight the importance of considering gender and the developmental timing of maltreatment. For ALDH2, the results indicated that maltreated girls evidenced significantly lower methylation compared to nonmaltreated girls, and maltreated boys evidenced significantly higher methylation compared to nonmaltreated boys. Moreover, early onset–not recently maltreated boys evidenced significantly higher methylation at ALDH2 compared to nonmaltreated boys. Similarly, children with early onset–nonrecent maltreatment evidenced significantly higher methylation compared to nonmaltreated children at ANKK1. The site-specific results were not altered by controlling for genotypic variation of respective genes. The findings demonstrate increased risk for adverse physical and mental health outcomes associated with differences in methylation in maltreated children and indicate differences among maltreated children related to developmental timing of maltreatment and gender in genes involved in mental health functioning.

A genome-wide methylation study was conducted among a sample of 114 infants (M age = 13.2 months, SD = 1.08) of low-income urban women with (n = 73) and without (n = 41) major depressive disorder. The Illumina HumanMethylation450 BeadChip array with a GenomeStudio Methylation Module and Illumina Custom model were used to conduct differential methylation analyses. Using the 5.0 × 10–7p value, 2,119 loci were found to be significantly different between infants of depressed and nondepressed mothers. Infants of depressed mothers had greater methylation at low methylation sites (0%–29%) compared to infants of nondepressed mothers. At high levels of methylation (70%–100%), the infants of depressed mothers were predominantly hypomethylated. The mean difference in methylation between the infants of depressed and infants of nondepressed mothers was 5.23%. Disease by biomarker analyses were also conducted using GeneGo MetaCore Software. The results indicated significant cancer-related differences in biomarker networks such as prostatic neoplasms, ovarian and breast neoplasms, and colonic neoplasms. The results of a process networks analysis indicated significant differences in process networks associated with neuronal development and central nervous system functioning, as well as cardiac development between infants of depressed and nondepressed mothers. These findings indicate that early in development, infants of mothers with major depressive disorder evince epigenetic differences relative to infants of well mothers that suggest risk for later adverse health outcomes.

The present study applies a multilevel approach to an examination of the effect of two randomized preventive interventions with mothers in neglectful families who are also contending with elevated levels of impoverishment and ecological risk. Specifically, we examined how participation in either child–parent psychotherapy (CPP) or psychoeducational parenting intervention (PPI) was associated with reductions in maternal psychological parenting stress and in turn physiological stress system functioning when compared to mothers involved in standard community services as well as a demographic comparison group of nonmaltreating mothers. The resulting group sizes in the current investigation were 44 for CPP, 34 for PPI, 27 for community services, and 52 for nonmaltreating mothers. Mothers and their 13-month-old infants were randomly assigned to intervention group at baseline. Mothers completed assessments on stress within the parenting role at baseline and postintervention. Basal cortisol was sampled at postintervention and 1-year follow-up. Latent difference score analyses examined change in these constructs over time. Results suggested that mothers within the CPP intervention experienced significant declines in child-related parenting stress, while mothers in the PPI intervention reported declines in parent-related parenting stress. In turn, significant decreases in stress within the CPP mothers were further associated with adaptive basal cortisol functioning at 1-year postintervention. The results highlight the value of delineating how participation in preventive interventions aimed at ameliorating child maltreatment in neglectful families within the context of poverty may operate through improvements in psychological and physiological stress functioning. Findings are discussed with respect to the importance of multilevel assessments of intervention process and outcome.

Child maltreatment is associated with disruptions in physiological arousal, emotion regulation, and defensive responses to cues of threat and distress, as well as increased risk for callous unemotional (CU) traits and externalizing behavior. Developmental models of CU traits have focused on biological and genetic risk factors that contribute to hypoarousal and antisocial behavior, but have focused less on environmental influences (Blair, 2004; Daversa, 2010; Hare, Frazell, & Cox, 1978; Krueger, 2000; Shirtcliff et al., 2009; Viding, Fontaine, & McCrory, 2012). The aim of the present investigation was to measure the independent and combined effects of child maltreatment and high CU traits on emotion-modulated startle response in children. Participants consisted of 132 low-income maltreated (n = 60) and nonmaltreated (n = 72) children between 8 and 12 years old who attended a summer camp program. Acoustic startle response (ASR) was elicited in response to a 110-dB 50-ms probe while children viewed a slideshow of pleasant, neutral, and unpleasant IAPS images. Maltreatment status was assessed through examination of Department of Human Services records. CU traits were measured using counselor reports from the Inventory of Callous and Unemotional Traits (Frick, 2004), and conduct problems were measured using counselor and child self-report. We found no significant differences in emotion-modulated startle in the overall sample. However, significant differences in ASR by maltreatment status, maltreatment subtype, and level of CU traits were apparent. Results indicated differential physiological responses for maltreated and nonmaltreated children based on CU traits, including a pathway of hypoarousal for nonmaltreated/high CU children that differed markedly from a more normative physiological trajectory for maltreated/high CU children. Further, we found heightened ASR for emotionally and physically neglected children with high CU and elevated antisocial behavior in these children. Results provide further support for differential trajectories by which experience and biology may influence the development of antisocial behavior in youth and highlight potential avenues for intervention.

Childhood maltreatment is a serious individual, familial, and societal threat that compromises healthy development and is associated with lasting alterations to emotion perception, processing, and regulation (Cicchetti & Curtis, 2005; Pollak, Cicchetti, Hornung, & Reed, 2000; Pollak & Tolley-Schell, 2003). Individuals with a history of maltreatment show altered structural and functional brain development in both frontal and limbic structures (Hart & Rubia, 2012). In particular, previous research has identified hyperactive amygdala responsivity associated with childhood maltreatment (e.g., Dannlowski et al., 2012). However, less is known about the impact of maltreatment on the relationship between the amygdala and other brain regions. The present study employed an emotion processing functional magnetic resonance imaging task to examine task-based activation and functional connectivity in adults who experienced maltreatment as children. The sample included adults with a history of substantiated childhood maltreatment (n = 33) and comparison adults (n = 38) who were well matched on demographic variables, all of whom have been studied prospectively since childhood. The maltreated group exhibited greater activation than comparison participants in the prefrontal cortex and basal ganglia. In addition, maltreated adults showed increased amygdala connectivity with the hippocampus and prefrontal cortex. The results suggest that the intense early stress of childhood maltreatment is associated with lasting alterations to frontolimbic circuitry.

A model examining the effects of an increasing number of maltreatment subtypes experienced on antisocial behavior, as mediated by impulsivity and moderated by a polygenic index of dopaminergic genotypes, was investigated. An African American sample of children (N = 1,012, M age = 10.07) with and without maltreatment histories participated. Indicators of aggression, delinquency, and disruptive peer behavior were obtained from peer- and counselor-rated measures to form a latent variable of antisocial behavior; impulsivity was assessed by counselor report. Five genotypes in four dopaminergic genes (dopamine receptors D4, D2, known as DRD4, DRD2; dopamine active transporter 1, known as DAT1; and catechol-O-methyltransferase, known as COMT) conferring heightened environmental sensitivity were combined into one polygenic index. Using structural equation modeling, a first-stage, moderated-mediation model was evaluated. Age and sex were entered as covariates, both as main effects and in interaction with maltreatment and the gene index. The model had excellent fit: χ2 (32, N = 1,012) = 86.51, p < .001; comparative fit index = 0.982, Tucker–Lewis index = 0.977, root mean square error of approximation = 0.041, and standardized root mean square residual = 0.022. The effect of maltreatment subtypes on antisocial behavior was partially mediated by impulsivity (β = 0.173, p < .001), and these relations were moderated by the number of differentiating dopaminergic genotypes. Specifically, a significant Gene × Environment interaction (β = 0.016, p = .013) indicated that the relation between maltreatment and impulsivity was stronger as children evinced more differentiating genotypes, thereby strengthening the mediational effect of impulsivity on antisocial behavior. These findings elucidate the manner by which maltreated children develop early signs of antisocial behavior, and the genetic mechanisms involved in greater vulnerability for maladaptation in impulse control within the context of child maltreatment.

The current study examined the prospective association between child maltreatment and the development of substance use disorder in adolescence with the aim of investigating pathways underlying this relation, as well as genetic moderation of these developmental mechanisms. Specifically, we tested whether youth who experienced maltreatment prior to age 8 were at risk for the development of marijuana dependence in adolescence by way of a childhood externalizing pathway and a childhood internalizing pathway. Moreover, we tested whether variation in FK506 binding protein 5 gene (FKBP5) CATT haplotype moderated these pathways. The participants were 326 children (n =179 maltreated; n = 147 nonmaltreated) assessed across two waves of data collection (childhood: ages 7–9 and adolescence: ages 15–18). Results indicated that higher levels of child externalizing symptoms significantly mediated the effect of child maltreatment on adolescent marijuana dependence symptoms for individuals with one or two copies of the FKBP5 CATT haplotype only. We did not find support for an internalizing pathway from child maltreatment to adolescent marijuana dependence, nor did we find evidence of moderation of the internalizing pathway by FKBP5 haplotype variation. Findings extend previous research by demonstrating that whether a maltreated child will traverse an externalizing pathway toward substance use disorder in adolescence is dependent on FKBP5 genetic variation.